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Biotech news from around the world.

Mitochondrial Proteostasis Links Diabetes and Sarcopenia: Cross-Scale Convergence from Experimental Models to Human Multi-Omics.

Wei Shibo S, Shin Soyeon S, Ryu Dongryeol D, Oh Chang-Myung CM

Sarcopenia in type 2 diabetes mellitus is increasingly recognized as a mechanistic consequence of chronic metabolic stress rather than mere age-related comorbidity. This review synthesizes evidence demonstrating how insulin resistance, hyperglycemia, lipotoxicity, and inflammation converge on skeletal muscle mitochondrial proteostasis to drive progressive decline. We evaluate seven pathway modules-mitochondrial dynamics, mitophagy, biogenesis, oxidative phosphorylation, nicotinamide adenine dinucleotide (NAD+)/sirtuin (SIRT)-linked regulation, protein import, and the mitochondrial unfolded protein response (UPRmt)-across an evidence map encompassing basic, clinical, and multi-omics studies. Dynamics and mitophagy represent mechanistically central quality-control nodes; their impairment permits dysfunctional organelle accumulation and promotes atrophic cascades. Direct evidence density, however, remains weighted toward oxidative phosphorylation and mitochondrial biogenesis. NAD+/SIRT-linked regulation, protein import fidelity, and UPRmt represent mechanistically upstream but comparatively underinvestigated signals. We propose a diabetes-centered framework where mitochondrial proteostasis failure mediates atrophy and reinforces insulin resistance via a self-amplifying feed-forward loop, supported by pathway responsiveness to coherent interventions. Human multi-omics data highlight network-level dysregulation rather than isolated defects, underscoring module-based biomarker strategies. Translationally, exercise remains the mechanistic cornerstone, while pathway-directed adjuncts-NAD+ precursor repletion, mitophagy modulators, and emerging pharmacotherapeutics-are warranted for patients with identifiable module-specific failure patterns.

Apparent metabolizable energy of black soldier fly larval meal and its effects on nutrient utilization in broiler diets.

Jiang Qiang Q, Zhou Zirui Z, Lei Jiaqi J, Zhu Qiaoli Q et al.

Black soldier fly larvae (BSFL) are a promising alternative protein source for use in animal feeds. This study aimed to measure the apparent metabolizable energy (AME) and nitrogen-corrected apparent metabolizable energy (AMEn) of defatted (161 g kg-1 ether extract) and full-fat (438 g kg-1 ether extract) BSFL, and evaluated the effects of their dietary inclusion on nutrient utilization in broilers. A total of 108 28-day-old Shengze 901 male broilers were randomly assigned to the control group (CON; basal diet), the defatted BSFL group (DF; defatted BSFL replacing 150 g kg⁻¹ of the basal diet), and the full-fat BSFL group (FF; full-fat BSFL replacing 150 g kg⁻¹ of the basal diet), with 6 cages of 6 birds each. The AME and AMEn (dry matter basis) of defatted BSFL were 9.11 and 8.58 MJ kg-1, whereas those of full-fat BSFL were 18.93 and 17.43 MJ kg-1, respectively. Both BSFL diets increased crude fiber digestibility and decreased ash digestibility (P < 0.05). The DF group had lower dry matter, crude protein, and gross energy digestibility than FF and CON groups (P < 0.05), and the FF group had higher crude protein digestibility than both other groups (P < 0.05). The DF group exhibited higher nitrogen excretion, lower nitrogen retention, and elevated uric acid, whereas the FF group showed the opposite. This study determined the AME and AMEn of defatted and full-fat BSFL. The FF group showed higher nitrogen utilization, highlighting the advantage of full-fat BSFL as a protein and energy source for broilers, whereas the higher nitrogen excretion of the DF group suggests cautious inclusion of defatted BSFL. © 2026 Society of Chemical Industry.

Insulin-like growth factor receptor signaling in physiology and disease.

Dilawar Muhammad M, Malik Anoosha A, Liao Junguang J, Shen Panpan P et al.

The insulin-like growth factor (IGF) signaling pathway plays a pivotal role in regulating a myriad of cellular and physiological processes, including cell proliferation, differentiation, and the maintenance of redox homeostasis. This review provides a comprehensive overview of the IGF/IGF receptor (IGFR) signaling axis, outlining its historical milestones and delineating its evolution from foundational discoveries to contemporary advancements. We elucidate the structural components of pathway, including ligands, receptors, and IGF-binding proteins, and discuss how multilevel regulation integrates upstream signals with downstream effectors such as the PI3K-AKT and MAPK/ERK pathways. Particular emphasis is placed on the crosstalk between IGF signaling and other pathways, including insulin, EGFR, PDGFR, VEGF, Wnt/β-catenin, JAK-STAT, and TGF-β/BMP in homeostasis and pathophysiological processes. We further discuss the role of IGF signaling in pathological process, highlighting insights from animal models and its implication in a wide range of human diseases, including cancer, cardiovascular diseases, neurodegenerative conditions, metabolic syndromes, skeletal abnormalities, and autoimmune and rare genetic disorders. Finally, we examine the therapeutic potential of targeting the IGF/IGFR axis, current clinical research advancements, FDA-approved pharmacological agents, and ongoing clinical trials. By incorporating historical insights with up-to-date scientific breakthroughs, our review underscores the need for systems-level and context-specific approaches to better understand IGF signaling dynamics, thus paving the way for the development of precision and personalized therapeutic strategies.